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作 者:毕铭霞[1,2] 朱彬[2] 张瑞斌[2] 逄曙光[3]
机构地区:[1]山东大学医学院,济南250012 [2]山东大学附属济南市中心医院血液净化中心,济南250013 [3]山东大学附属济南市中心医院内分泌科,济南250013
出 处:《山东大学学报(医学版)》2011年第1期6-9,13,共5页Journal of Shandong University:Health Sciences
摘 要:目的观察饮食中晚期糖基化终产物(AGEs)对糖尿病肾病(DN)大鼠肾脏的影响,探讨其作用机制。方法 SD大鼠40只,随机选取10只为空白对照组,30只大鼠DN模型建立成功,随机分为3组:高AGEs饲料组、低AGEs饲料组及普通饲料组,每组10只。分别于第9周及第13周对各组大鼠进行检测:考马斯亮蓝法测定24h尿蛋白量,速率法测定血肌酐(Scr)和尿肌酐,硫代巴比妥酸反应法(TBARS)测定24h尿及肾组织匀浆中丙二醛(MDA)含量,ELISA法测定血清及肾组织匀浆中羧甲基赖氨酸(CML)含量,比色法测定血清及肾组织匀浆中硒谷胱甘肽过氧化物酶(SeGSHPx)活性,计算内生肌酐清除率(Ccr)。结果 3组DN大鼠各指标与空白对照组相比,差异有统计学意义(P<0.05)。与普通饲料组相比,高AGEs饲料组大鼠24h尿蛋白、24h尿及肾组织匀浆中MDA含量、血清及肾组织匀浆中CML含量显著增加(P<0.05),血清及肾组织匀浆中SeGSHPx活性显著降低(P<0.05);低AGEs饲料组大鼠24h尿蛋白、24h尿及肾组织匀浆中MDA含量、血清及肾组织匀浆中CML含量显著减少(P<0.05),血清及肾组织匀浆中SeGSHPx活性显著升高(P<0.05)。3组DN大鼠之间Scr及Ccr差异无统计学意义(P>0.05)。结论高AGEs饲料促进DN大鼠肾功能恶化,其作用机制与抗氧化体系受损、氧化应激增强有关。Objective To study the effect of oral advanced glycation end products(AGEs) on rats with diabetic nephropathy(DN) and its mechanism.Methods 10 rats were randomly selected from 40 male Sprague-Dawley rats as the control group.The other 30 rats which developed DN were randomly divided into three groups: the AGEs-rich diet group,the AGEs-poor diet group and the common diet group,10 rats in each group.Each group was studied at the 9th and 13th weeks.The following parameters were detected with different methods: 24 h urinary albumin with the Coomassie brilliant blue method,serum creatinine and urine creatinine by an automatic biochemistry analyzer,content of MDA in 24 h urine and nephridial tissue homogenate by TBARS,content of CML in serum and nephridial tissue homogenate by ELISA,and activity of SeGSHPx in serum and nephridial tissue homogenate by a spectrophotometer.Ccr wascalculated.Results Significant differences were found between the three DN groups and the control group(P 〈0.05).Compared to the common diet group,the following variables in the AGEs-rich diet group were dramatically increased: the 24 h urine protein,MDA levels in 24 h urine and nephridial tissue homogenate,and CML levels in serum and nephridial tissue homogenate(P 〈0.05);while SeGSHPx activities in serum and nephridial tissue homogenate decreased(P 〈0.05).In contrast,the AGEs-poor diet group showed opposite results in all the above variables.No significant difference was observed in Scr and Ccr among the three DN rat groups(P 〉0.05).Conclusion An AGEs-rich diet impairs the renal function of DN rats and the mechanism is probably related to damage to anti-oxidation ability and enhancement of oxidative stress.
关 键 词:晚期糖基化终产物 糖尿病肾病 氧化应激 丙二醛 硒谷胱甘肽过氧化物酶
分 类 号:R332[医药卫生—人体生理学]
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